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@ARTICLE{KlingerKnig:140563,
      author       = {Klinger-König, Johanna and Hertel, Johannes and Van der
                      Auwera, Sandra and Frenzel, Stefan and Pfeiffer, Liliane and
                      Waldenberger, Melanie and Golchert, Janine and Teumer,
                      Alexander and Nauck, Matthias and Homuth, Georg and Völzke,
                      Henry and Grabe, Hans J},
      title        = {{M}ethylation of the {FKBP}5 gene in association with
                      {FKBP}5 genotypes, childhood maltreatment and depression.},
      journal      = {Neuropsychopharmacology},
      volume       = {44},
      number       = {5},
      issn         = {0893-133X},
      address      = {Basingstoke},
      publisher    = {Nature Publishing Group71819},
      reportid     = {DZNE-2020-06885},
      pages        = {930-938},
      year         = {2019},
      abstract     = {DNA methylation of the FKBP5 gene is assumed to alter FKBP5
                      expression and hence the synthesis of the FK506 binding
                      protein 51, a central element of a genomic negative feedback
                      loop for glucocorticoid receptor signaling. The present
                      study aimed to replicate and extend previously reported
                      influences of FKBP5 genotypes, childhood maltreatment and
                      depression on methylation levels of five CpG sites in intron
                      7 of the FKBP5 gene in a large population-based sample.
                      Besides the single nucleotide polymorphism (SNP) rs1360780,
                      associations of the FKBP5 methylation with 22 other,
                      unlinked FKBP5 SNPs as well as associations between FKBP5
                      methylation levels and transcription levels were
                      investigated. Using whole-blood methylation of 3965 subjects
                      of the Study of Health in Pomerania (SHIP) reduced
                      methylation levels in TT allele carriers of rs1360780
                      (OR = 0.975, p = .005) and currently depressed
                      subjects (OR = 0.995, p = 0.005) were found.
                      Further, an impact of two yet undescribed SNPs (rs6910300,
                      rs7771727) on methylation levels was observed. However, main
                      and interactive effects for childhood maltreatment and
                      lifetime major depressive disorder observed in previous
                      studies could not be replicated. Finally, FKBP5 methylation
                      levels were not related to FKBP5 transcription levels in
                      whole blood. Thus, the present study verified the
                      associations of FKBP5 genotypes and state depression on the
                      FKBP5 methylation levels of five CpG sites in intron 7.
                      However, FKBP5 methylation of these five CpG sites could not
                      be validated as a valuable clinical biomarker for biological
                      long-term effects of childhood maltreatment or lifetime
                      depression.},
      keywords     = {Adult / Adult Survivors of Child Abuse: statistics $\&$
                      numerical data / Adverse Childhood Experiences: statistics
                      $\&$ numerical data / Aged / DNA Methylation: genetics /
                      Depressive Disorder: epidemiology / Depressive Disorder:
                      etiology / Depressive Disorder: genetics / Female /
                      Follow-Up Studies / Germany: epidemiology / Humans / Male /
                      Middle Aged / Registries / Tacrolimus Binding Proteins:
                      genetics / Young Adult / Tacrolimus Binding Proteins (NLM
                      Chemicals) / tacrolimus binding protein 5 (NLM Chemicals)},
      cin          = {AG Grabe},
      ddc          = {610},
      cid          = {I:(DE-2719)5000001},
      pnm          = {344 - Clinical and Health Care Research (POF3-344)},
      pid          = {G:(DE-HGF)POF3-344},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:30700816},
      pmc          = {pmc:PMC6461917},
      doi          = {10.1038/s41386-019-0319-6},
      url          = {https://pub.dzne.de/record/140563},
}